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Review Articles
IMAGING IN ABDOMINAL
TUBERCULOSIS
Imágenes en tuberculosis abdominal
Tatiana Suárez1
Vanessa García2
Tamara Estrada3
Federico Acosta3
Key words (MeSH)
Tuberculosis
Tuberculosis renal
Tuberculosis hepatic
Tuberculosis splenic
Tomography, x-ray
computed
Palabras clave (DeCS)
SUMMARY
In this article we illustrate and discuss the imaging characteristics of abdominal
tuberculosis. We present a group of patients assessed with abdominal symptoms and
findings suggesting granulomatous disease, using several imaging modalities. The
diagnosis was confirmed on the basis of the clinical and histopathological findings.
Cases include involvement of several abdominal organs such as the lymphatic system,
peritoneum, liver, spleen, kidneys, ureters and pelvic organs.
Tuberculosis
Tuberculosis renal
Resumen
Tuberculosis hepática
En este artículo se discuten e ilustran las características por imagen de la afectación
Tuberculosis esplénica
abdominal
por tuberculosis. Se presenta un grupo de pacientes evaluados a través de diTomografía computarizada
ferentes
modalidades
diagnósticas con síntomas abdominales y hallazgos imaginológicos
por rayos x
sugestivos de infección granulomatosa. Este diagnóstico fue confirmado posteriormente
en la evolución clínica y con estudio histológico. Se incluyen casos de afectación en diferentes órganos abdominales, como sistema linfático, peritoneo, órganos pélvicos, hígado,
bazo, riñones y uréteres.
Introduction
Radiologist. Hospital San Vicente de Paúl.
Professor of Radiology, Universidad de
Antioquia. Medellín, Colombia.
2
Radiologist, Hospital Pablo Tobón Uribe.
Professor of Radiology, Universidad de
Antioquia. Medellín, Colombia
3
Radiology Resident, Universidad de
Antioquia. Medellín, Colombia.
1
Rev Colomb Radiol. 2010; 21:(4):1-11
Abdominal tuberculosis is defined as the
isolated or combined involvement of the gastrointestinal tract, peritoneum, omentum, abdominal
lymph nodes and solid organs, as a result of the
disease (1). Because it mimics different conditions
such as proliferative lymph node disease, storage
and autoimmune diseases, abdominal tuberculosis
it is difficult to diagnose. Consequently, histopathology is required to confirm the diagnosis,
although in cases of a proven focus of tuberculosis
in a different organ (lungs), abdominal findings
may be accepted as secondary to this disease (2).
The lung is the organ most commonly involved, considering that abdominal extension
is found in only 10% of cases – although this
percentage is higher in patients with immune
disorders (2). Solid organs are more commonly
affected than hollow viscera (1). In most patients
with abdominal tuberculosis there is an existing
lung focus, identified or not in imaging studies,
and the tuberculin test is usually negative, making
the diagnosis still more difficult.
Abdominal tuberculosis is more frequent
between the third and fourth decades of life. Abdominal infection routes include spread through
the bloodstream from a primary pulmonary focus,
miliary tuberculosis (with propagation through
the infected lymph nodes), intake of the mycobacterium (from sputum or other infected sources
such as dairy products), and direct extension into
adjacent organs. Peritoneal and abdominal lymph
node involvement may occur without compromising other organs (3,4). It is important to know the
1
patient’s history of infection, epidemiological risk and immune
status, because imaging findings of abdominal tuberculosis are
non-specific.
Nodal tuberculosis
Lymphadenitis is the most frequent manifestation of intraabdominal tuberculosis and is present in 9% to 93% of cases (5).
It usually affects periportal lymph nodes, followed by peripancreatic, inter-aortocaval and mesenteric nodes (6). This is due
to the fact that the drainage sites of the organs most commonly
affected by tuberculosis are the ileocecal region, right colon,
liver and spleen. It may be the only manifestation of tuberculosis.
The routes of dissemination to the lymph nodes include the
intake of contaminated food, the bloodstream and the lymphatic
system. Lymph node size and appearance vary, with sizes ranging between 1 and 2-4 cm, indicating self-limiting growth. Additionally, they are usually lobulated and clustered. Periportal
lymph node involvement manifests as obstructive jaundice,
thrombosis or portal hypertension. Cases of renal vascular hypertension have been described because of compression of the
renal arteries by the lymph node disease.
In patients with HIV infection in AIDS stage, lymphatic
spread is more frequent with involvement of more than one
lymph node chain. These patients also suffer more often from
generalized symptoms such as fever, sweating and weight loss.
From a histopathological point of view, there are several
stages in the disease: lymphoid hyperplasia, caseification necrosis, capsular destruction, cold abscess formation, and cure with
fibrosis and calcification. The imaging appearance of the lymph
node disease depends on the pathological phase of the nodes:
On ultrasound, the nodes appear hypoechoic with a more
hypoechoic core due to caseification. In a late phase they appear calcified.
On computed tomography (CT) they appear hypodense,
mainly at the core, and contrast scans reveal their presence in the
periphery, in the non-caseified area. This enhancement pattern
is the most frequent and characteristic in tuberculosis, although
it is not pathognomonic (Figure 1). This same pattern may be
seen in mestastatic disease in the ovaries and testicles, lymphoma
(especially after treatment), Crohn’s disease, sarcoidosis, and
Whipple and Castleman disease.
Other imaging patterns in tuberculous nodal disease include
homogenous enhancement or non-enhancement (Figure 2). Magnetic resonance imaging (MRI) may also suggest tuberculous
findings when lymphadenopathies appear in the form of confluent masses with central necrosis, accompanied by edema of the
surrounding soft tissues. The enhancement pattern is similar
to that seen on CT, with central liquefaction. The nodes may
appear hypointense in T2 due to the presence of free radicals,
secondary to caseification necrosis.
Genitourinary tuberculosis
After lymphadenopathy, the urinary tract is the second system most often compromised in extrapulmonary tuberculosis (7).
All the organs in the system may be involved: kidneys, ureters,
2
Figure 1. Contrast abdominal CT in the portal phase in a 32 year-old male showing multiple
mesenteric and retroperitoneal lymphadenopathies with hypointense cores and peripheral
enhancement (arrows). No other organs were involved.
Figure 2. Contrast abdominal CT and coronal reconstruction with maximum intensity view
of a 48 year-old male. Nodal disease was found in multiple non-enhancing hypogastric,
inguinal and mesenteric node chains (arrows) with no necrotic cores.
bladder, uterus, cervix, adnexa, prostate, testicles, epididymus
and seminal vesicles. It is a significant, though infrequent form
of tuberculosis.
It is found in 2% to 20% of all patients with pulmonary
tuberculosis. Symptoms are non-specific, leading to late diagnosis and treatment. It is frequently associated with secondary
renal failure and destruction or urogenital organs (8). The most
important clinical manifestation is the presence of hematuria,
which only occurs when the infection affects the bladder in very
advanced stages of the disease (9).
Genitourinary tuberculosis occurs as a result of the bloodborne spread of the mycobacterium from the lung to the renal
capillaries. Later on, the mycobacerium filters through the urine
and colonizes the urothelium. Granulomas are formed inside
the renal parenchyma and the mycobacterium may remain
Imaging in abdominal tuberculosis, Suárez T, García V, Estrada T, Acosta F
Review Articles
dormant for years and then become activated as a result of any
immune disorder. Granulomas may extend to the medulla, then
to the papillae and finally break inside the collecting cavities.
The prostate and epididymus are infected through bloodstream
spread, while the testicles, cervix and seminal vesicles become
involved by direct extension from the genitourinary tract (10).
The mycobacterium has been found in the urine of only 1520% of patients with tuberculosis infection, although not all of
them develop the infection. The probability of developing the
infection depends on the size of the inoculum, the virulence
of the mycobacterium and the patient’s immune status. People
with HIV or transplants are at risk for renal tuberculosis because
the probability is three times as high as in immunocompentent
patients, and their manifestations are more severe, with higher
parenchymal and systemic involvement (11).
Type II. Hydronephrosis. Accounts for 14% of cases of renal
tuberculosis. There is dilatation of the renal pelvis and collecting
cavities. The urothelial walls appear thickened and echogenic.
Type III. Empyema. It is present in 8% of cases. The kidney
appears enlarged and hypoechoic. At the same time, the cavities
are distended with echogenic material inside.
Type IV. Atrophy and inflammation. Found in 10% of cases.
The kidney is reduced in size and shows irregular contours.
Findings are similar to those of chronic nephropathy, but they
are unilateral.
Type V. Calcification. It accounts for 22% of cases. The
kidney is markedly reduced in size with a thin cortical area
and multiple areas of dysmorphic calcification replacing the
parenchyma (Figure 3).
Renal tuberculosis
Once the mycobacterium reaches the renal capillaries, it
forms small granulomas that give rise to the miliary form of the
disease, which is usually bilateral, and is missed in patients with
adequate immunity. The latency period for this miliary infection ranges between 1 and 47 years. After the latency period, if
there is any immune alteration, the mycobacterium may infect
the rest of the renal parenchyma in an insidious and destructive
way, which is usually asymmetrical (destruction is bilateral in
up to 30% of cases).
In the acute phase of the infection, the kidney may appear
normal on imaging or enlarged because of the growth and
coalescence of the granulomas, which appear hypoechoic on
ultrasound (US) and hypodense on CT. As the disease advances,
renal function declines, and there is delay in uptake, concentration and washout of the contrast medium.
The extension of the disease to the medulla produces papillary necrosis, a characteristic but non-specific finding in renal
tuberculosis. On ultrasound, it appears in the form of swollen and
hypoechoic papillae due to cavitation or secondary detachment;
in the urogram and on CT, it is frequent to find papillae with a
moth-eaten appearance. In the late phases, residual calcifications
are the main presentation (50%) in the form of stones, caseous
debris or replacement of the entire renal parenchyma, giving
rise to autonephrectomy.
The collecting cavities and the renal pelvis may show
obstruction and tortuousness secondary to areas of stenosis,
or calcifications in the cavities. At the same time, residual calcifications and obstructive uropathy lead to total loss of renal
function. It is important to bear in mid that a solid mass may be
a manifestation of renal tuberculosis; in this case, the differential
diagnosis is a neoplastic lesion, and histology is required.
Xuefang Rui et al. assessed 258 patients with renal tuberculosis and proposed a classification of ultrasound finding into
five stages, according to the pathological course (12):
Type I. Nephrectasia. Found in 15% of patients. The capsule
is irregular and the renal parenchyma shows multiple, poorlydefined, hypoechoic areas. It may be associated with complex,
thick-walled cysts.
Rev Colomb Radiol. 2010; 21:(4):1-11
Figure 3. Contrast abdominal CT in a 62 year-old male. There is evidence of severe renal
atrophy and peripheral calcification of the entire renal cortex as a result of chronic type IV
(mixed) tuberculosis. It occurs in 34% of cases. The size of the kidney is variable and it shows
lobulated contours. There are hypoechoic areas associated with calcifications (arrow).
In summary, urographic and CT-scan findings of renal
tuberculosis include moth-eaten calices, parenchymal mass,
amputated infundibula, autonephrectomy, thickening of urinary
tract walls, parenchymal and cavity calcifications, cavities in
the renal parenchyma, hydrocalcinosis, hydronephrosis and
hydroureter secondary to segmental stenosis (13).
Secondary amyloidosis may occur in tuberculosis or any
other chronic inflammatory disease associated with high concentrations of acute-phase reactants, such as Type A amyloid
protein. This disease must be suspected in all patients with
tuberculosis beginning with proteinuria, generally within the
nephrotic range. The diagnosis is confirmed once amyloid
deposits are documented in the renal biopsy (14). Likewise, it
is important to take into consideration differential diagnoses
for renal tuberculosis, including fungal or drug-related chronic
pyelonephritis, renal ischemia and lymphoma.
Ureteral tuberculosis
Continuous renal parenchymal involvement leads to bacilluria secondary to the rupture of the renal granulomas into the
collecting cavities. This produces a descending infection that
3
travels through the collecting system. Ureteral involvement is
found in up to 50% of cases of renal tuberculosis (15).
At first there is inflammatory thickening of the urothelium
followed by areas of stenosis and residual fibrosis. The areas
with greatest compromise are the phyisiologically narrow areas
of the ureter: the uretoropelvic and ureterovesical junctions and
the middle third at the vascular crossing, because urine stasis
increases the contact between the mycobacterium and the walls
of the ureter. These stenoses are usually short and multiple
(Figure 4).
Figure 4. Volume rendering of an elimination-phase urotomography in a young 19 year-old
female. There is evidence of two short segmental stenoses in the left distal ureter (arrow)
with proximal dilatation and secondary hydronephrosis (asterisk); additionally, bladder
capacity is reduced and shows irregular contours (arrow head) due to bladder and left
ureteral tuberculosis.
The ureter may appear dilated as a result of the stenotic areas or because of vesicoureteral reflux, secondary to bacilluria
(16). There may also be multiple extensive calcifications in the
ureteral tract, giving the appearance of a pipeline ureter.
Bladder tuberculosis
In general, the kidney is affected before the bladder, although
there have been case reports of tuberculous cystitis without prior
renal infection (17). Clinically, there is evidence of hematuria,
dysuria and urgent incontinence. In principle, the contaminated
urine produces an acute inflammatory process with hyperemia,
ulceration, tubercle formation in the area close to the trigone,
and subsequent transmural fibrosis (18).
Imaging findings include thickening, mural irregularity
and calcifications, reduced bladder capacity and ulcers. On
occasions, the disease may manifest in the form submucosal
masses mimicking a transitional-cell carcinoma (Figure 5).
Other differential diagnoses include schistosomiasis and drug
or radiation-associated cystitis (19). In advanced stages of the
disease, these patients may require a surgical procedure, like
4
the creation of a neobladder, because bladder capacity may be
extremely compromised.
Genital tuberculosis
Genital tuberculosis is rare. There are no imaging findings or
specific clinical findings, and the consequences are catastrophic.
The problem is compounded by a very high rate of female
infertility (up to 73%). Spread to these organs is usually blood
borne or results from contiguity, although sexually-transmitted
infections have also been described (20).
In women, the disease involves the Fallopian tubes in most
cases (94%) and usually causes bilateral salpingitis. Other
manifestations include menstrual cycle alterations, amenorrhea,
infertility, Bartolino gland inflammation with fistula formation,
cervical erosions and endometrial thickening. These findings
cannot be distinguished from a neoplasm (21). The clinical
manifestations may be subtle and go unnoticed in the acute
phase, resulting in infertility later on.
Hysterosalpingography shows multiple tubal stenoses and
obstructions, endometrial adhesions or deformity of the cavity.
Other diagnostic modalities reveal calcified nodules, adnexal
calcifications and tubo-ovarian abscesses with extraperitoneal
extension, a finding that suggests pelvic tuberculosis (21) (Figure 6).
In males, tuberculosis affects mainly the seminal vesicles or
the prostate. Unlike what happens in women, it rarely causes
infertility, unless the involvement is bilateral (22). Tuberculous
prostatitis may mimic carcinoma, with a rise in prostatic antigen
values in 30% of cases and non-specific imaging appearance.
Consequently, a biopsy is required in order to make the diagnosis
in the majority of cases. On CT and US, it usually appears in
the form of hypodense or hypoechoic lesions, respectively, associated with necrotic areas and peripheral calcifications. These
lesions appear hyperenhanced with the use of contrast medium.
Magnetic resonance may show increased gland volume with a
“watermelon” sign on T2, where the gland appears hypointense
with high-signal striations, although this appearance is nonspecific (23).
The epididymus is one of the male genital organs most frequently affected by tuberculosis because of its rich blood supply.
It may also be affected through the lymphatic route, through
direct or retrograde extension. Involvement manifests itself in
the form of edema and scrotal pain. The portion usually affected
is the tail, and in most cases the involvement is unilateral. On
ultrasound, the epididymus appears enlarged, hypoechoic and
heterogenous. The involvement may also appear as a solid hypoechoic lesion, undistinguishable from a tumoral lesion (21).
Isolated testicular infections with no epididymal involvement
are rare. The testicle appears enlarged and hypoechoic, and its
margin cannot be distinguished from the epididymus.
Peritoneal tuberculosis
Although its true incidence has not been determined (24),
peritoneal tuberculosis is sixth among extrapulmonary manifestations of tuberculosis in the United States. The isolated form
Imaging in abdominal tuberculosis, Suárez T, García V, Estrada T, Acosta F
Review Articles
a
b
Figure 5. Abdominal ultrasound (a) and contrast abdominal late-phase CT (b) in a 65 yar-old male. Regular concentric thickening of the bladder mucosa (arrow) with a very reduced
repletion volume. Presence of a bladder catheter (asterisk). Bladder tuberculosis without renal damage.
b
c
a
Figure 6. Contrast abdominal CT with multiplanar axial (a), sagittal (b) and coronal (c) reconstructions in a 25 year-old woman. There is lymph node clustering in the pelvic region
and infiltration of the Fallopian tubes and ovaries. There is no cleavage plane with the uterus (asterisk). The distal third of the ureter is compromised with hydronephrosis (arrow). The
findings are consistent with pelvic peritonitis and secondary bilateral tubo-ovarian abscess due to tuberculosis.
is rare, and it is usually associated with extensive abdominal
disease (25). Usual associations include immune deficiency,
cirrhosis, alcoholism, diabetes, a history of peritoneal dialysis
and intravenous drug abuse. It is believed to spread through the
bloodstream, but it may occur due to gut perforation or extension
from the Fallopian tubes or the lymph nodes (26).
Clinical symptoms may include abdominal pain, bloating
and symptoms arising from other organs, including the lungs.
Involvement is divided into three types: wet, fibrous and dry.
These forms are frequently found together. Wet peritonitis is the
most common form of tuberculous peritonitis and consists of free
or septated ascites (Figure 7). The second type is fibrous peritonitis, characterized by large omentum and mesenteric masses
with fixed intestinal loops. The dry form is less common and
Rev Colomb Radiol. 2010; 21:(4):1-11
consists of mesenteric thickening and lymph node caseification
(27) (Figure 8).
CT findings in tuberculous peritonitis include smooth thickening and enhancement of the peritoneum, thickened nodular
mesentery, high-density ascites (25-45 HU) and low-density
lymph nodes (28). The differential diagnosis includes peritoneal carcinomatosis, amyloidosis, peritoneal mesothelioma and
lymphoma (1).
Hepatic tuberculosis
Liver involvement is frequent in miliary tuberculosis. It
manifests as liver insufficiency and hepatomegaly. It may be
found on occasions in immunocompetent patients without lung
disease (29,30). In miliary tuberculosis, spread to the liver is
5
b
a
*
*
Figure 7. Contrast abdominal CT of a 10 year-old boy. (a) Axial view and (b) coronal reconstruction showing free ascitic fluid that appears hyperdense
(asterisk) when compared to urine (arrow), indicating high protein content. It is accompanied by mensenteric lymphadenopathies (arrow head)
and wet tuberculous peritonitis.
c
b
a
Figure 8. Contrast abdominal CT in a 38 year-old woman. (a) Axial section, (b) sagittal reconstruction and (c) coronal section showing thickening of the greater omentum and mesentery
(asterisk) that produces a desmoplastic reaction and tethering of the intestinal loops. The involvement extends to the pelvis (arrow) due to mixed fibrotic dry peritonitis.
through the hepatic artery. In its localized forms, the route of
propagation may be the portal vein (31).
The macronodular form (tuberculoma and abscesses) is infrequent and the diagnosis may be difficult when it occurs. The
most common symptoms include right upper quadrant pain, fever,
anorexia and weight loss (32). Elevated transaminases may be
present in two thirds of the cases. It is often accompanied by anemia and elevated globular sedimentation rate. CT findings include
multiple small hypodense nodules in the miliary form (Figure 9)
and gross calcification in the chronic stages. The macronodular
form presents with larger single or multiple hypodense non-enhancing nodules. These nodules may coalesce to form abscesses.
Biopsies of these lesions may reveal the presence of granulomas.
Tissue culture provides bacteriological confirmation (33).
The gall bladder is rarely infected with tuberculosis because
the normal mucosa and the wall of the gall bladder are resistant
to the mycobacterium. Involvement is usually associated with
6
severe abdominal tuberculosis affecting the peritoneum, the
mesentery and the lymph nodes. On imaging, the appearance
is non-specific, showing a thick-walled gall bladder or a central
soft tissue mass. It must be considered as part of the differential
diagnosis for gall bladder carcinoma or adenomyomatosis (34).
Splenic tuberculosis
The spleen is the fifth organ most commonly infected in miliary tuberculosis after the lung, the liver, the lymph nodes and
the bone marrow (35). Splenic tuberculosis occurs mainly in immunosuppressed patients. It manifests in the form of low-density
micronodules and splenomegaly on CT. On ultrasound there
is a diffuse increase in echogenicity and multiple hypoechoic
or echogenic nodules. Calcifications may be identified in the
chronic forms (1,5,36).
The differential diagnosis in the miliary form includes metastasis, lymphoma, sarcoidosis and fungal infection (37). Another
Imaging in abdominal tuberculosis, Suárez T, García V, Estrada T, Acosta F
Review Articles
Figure 9. Contrast abdominal CT (extreme window for better characterization of the
lesions) in a 40 year-old woman with miliary lung tuberculosis. The scan shows multiple
hypoattenuating micronodules in the liver parenchyma (arrows).
rare form is the macronodular form that manifests as a single
nodule (tuberculoma) or as multiple 1-3 cm nodules. On ultrasound, this lesion appears with variable echogenicity and on CT
it appears hypodense with minimal peripheral enhancement (1).
The primary isolated involvement of the spleen is rare.
However, there are some case reports in the literature (38,39),
all of them involving immunocompromised patients, with varying presentations of micronodular or macronodular patterns, or
tuberculous abscess (Figure 10).
Figure 10. Contrast abdominal CT of a 57 year-old immunosuppressed male patient. There
is evidence of a splenic abscess secondary to tuberculosis infection (asterisk), and abdominal
aortic tuberculosis (arrow). The diagnosis of isolated splenic tuberculosis is difficult and
usually late because of the non-specific clinical manifestations. For this reason, patients
are usually severely ill at the time of diagnosis and require splenectomy.
Adrenal tuberculosis
Adrenal tuberculosis occurs only in 6% of patients with active tuberculosis. In most cases it is bilateral but asymmetrical
(40). In the acute and subacute stages of the disease there is
evidence of diffuse and homogenous increase in the size of the
gland, or a hypodense core with peripheral enhancement, suggesting necrosis. It may also appear as a solid mass with nonspecific characteristics; however, a solid mass with preserved
glandular contours is more suggestive of granulomatous disease
rather than neoplasia (41).
In the later stages, the size of the gland diminishes and is
replaced by gross calcifications (Figure 11). The differential
diagnosis includes metastasis, lymphoma, primary neoplasia and
hemorrhage. Because of progressive destruction of both glands,
the clinical findings suggest Addison’s disease (42).
Pancreatic tuberculosis
Pancreatic tuberculosis is extremely rare and is normally
due to miliary propagation. It is more frequent in AIDS patients.
The lesion is found in the head or the neck of the pancreas,
although tail lesions have also been described. Clinical manifestations include weight loss, low-grade fever, anorexia and
upper abdominal pain. However, unlike pancreatic carcinoma,
pancreatic tuberculous lesions rarely produce back pain or
obstructive jaundice (43).
Rev Colomb Radiol. 2010; 21:(4):1-11
Figure 11. Contrast abdominal CT of an elderly, 73 year-old female patient, with a history
of pulmonary tuberculosis, previously treated. The left adrenal grand appears enlarged
with heterogenous uptake of the contrast medium and incomplete annular calcification
(thick arrow); ascitic (arrow head) and pleural (thin arrow) fluid. Residual left adrenal
tuberculosis.
Pancreatic tuberculosis may be focal or diffuse. In the focal
form, it appears as a poorly-defined mass, whereas in the diffuse
form there is and overall increase in gland size, with or without
stenosis of the main pancreatic duct.
On ultrasound, the lesion appears as a focal hypoechoic mass
and, on CT, it appears as a low-attenuation, peripherally-enhancing mass. An abscess may form on the site of the lesion and
later on it may be replaced by residual calcifications. Pancreatic
involvement due to tuberculosis may be associated frequently
with peripancreatic lymphadenopathies, making diagnosis much
more difficult. On MRI, the lesions appear hypointense in T1 and
hypo or hyperintense in T2. The common biliary duct and the
7
common pancreatic duct appear normal in the focal form, and
may appear stenotic in the diffuse form (44). In the majority of
cases, the diagnosis is made by histopathology because of the
need to rule out pancreatic carcinoma, focal chronic pancreatitis
and metastasis (45).
Intestinal tuberculosis
Intestinal tuberculosis is not very frequent and its incidence is
unknown: in close to 80% to 90% of all patients with abdominal
tuberculosis there is intestinal involvement. The mycobacterium
may also invade the gut mucosa through four different routes,
including swallowing infected sputum, bloodstream spread from
the lung, intake of contaminated food or milk, and contiguity
spread (46).
There is gross evidence of three lesional patterns: small
submucosal ulcers, pseudonodular hypertrophic lesions or a
mix of both patterns, and an ulcerated hypertrophic or “cobblestone” pattern, as shown with barium studies (47). Ulcers are
multiple, small, with poorly differentiated and raised edges,
usually larger than those found in Crohn’s disease. The regions
usually involved, in descending order, are the ileoceal valve,
ileum, caecum, ascending colon, jejunum, the rest of the colon,
rectum and duodenum, and the stomach.
On US there is evidence of concentric mural thickening of the
caecum and the ileum, edema and absence of peristalsis (Figure
12). Additional, though non-specific findings include ascites,
lymphadenopathies and thickening of the omentum. Abdominal
CT is the best test for assessing intra- and extraluminal involvement. The most frequent finding is asymmetrical thickening of
the ileocecal region and the medial wall of the colon, with or
without proximal intestinal dilatation. Lymphadenopathies are
multiple and appear hypodense in the center due to caseous
necrosis (Figure 13).
The differential diagnosis for this ileocecal valve involvement includes amebiasis, lymphoma, Crohn’s disease, cecal
Ileocecal tuberculosis
The most frequent location is the ileocecal region (90%).
This does not happen by accident and is explained on the basis of
the venolymphatic stasis and the abundance of lymphoid tissue
found in this area. The mycobacterium penetrates the mucosa
and remains in the submucosal lymphoid tissue where an inflammatory response is triggered, with lymphangitis, endarteritis,
granuloma formation, caseous necrosis and mucosal ulceration.
The clinical manifestations are highly non-specific and
include abdominal pain, anorexia, asthenia, fever, nocturnal
sweating, weight loss, diarrhea, constipation, rectal bleeding,
right iliac fossa mass, and ascites. The presence of ascites may
be a useful clue in differentiating this condition from Crohn’s
diease, where ascites is not a common finding.
Radiological signs are non-specific and the differential diagnosis with Crohn’s disease, lymphoma or cecal carcinoma is
difficult. Barium studies during the early stages may show spasm
and reactive hypermotility of the ileocecal valve, longitudinal
submucosal ulcers of the small intestine and transverse colonic
ulcers along the path of the lymphoid follicles, as well as ileocecal valve incompetence. In later stages there is thickening of the
valve lips and a larger gap between the valve and the thickened
terminal ileum (Fleischner’s sign).
In advanced states, due to fibrosis, there are symmetrical
annular stenoses (napkin ring) and obstruction associated with
tethering and shortening. The terminal ileum is narrow and stiff,
the ileocecal valve expands with a shortened tapered caecum
(Stierlin’s sign), representing acute inflammation overimposed on
chronic inflammation of the same segment. Later on there is cecal
retraction outside the iliac fossa into the hepatic flexure. Deep
fissures and fistulae may form in the final stages of the disease.
8
Figure 12. High-frequency linear-probe US of the right iliac fossa in a 28 year-old woman.
There is diffuse concentric thickening of the walls of the distal ileal loops and the caecum
(arrow).
carcinoma and sarcoidosis. Ileocecal tuberculosis may extend
to the appendix and produce acute or chronic appendicitis (48).
Endoscopic findings include ulcers, stenoses, pseudopolyps,
fibrous bands, fistulae and ileocecal valve deformity (49).
Esophageal tuberculosis
Esophageal tuberculosis is found most frequently in AIDS
patients and manifests in the form of dysphagia and painful
swallowing. It occurs by swallowing of infected sputum and
invasion into the mucosa, usually through a pre-existing mucosal
lesion. It may also occur through the bloodstream, lymphatic
drainage or direct invasion from the lymph nodes or the lungs.
Non-specific findings include esophagitis, mucosal thickening, ulcers, plaques, fistulae and stenoses, these latter two in the
late stages of the disease. There is also extrinsic compression
due to adjacent lymphadenopathies, mainly at the carina. In the
late stages there is diverticular formation due to traction resulting from chronic fibrotic changes and stenosis. CT is used to
determine mediastinal extension of the disease.
Gastric tuberculosis
Gastric involvement in tuberculosis is extremely rare
and is due to extension from the lymph nodes or through the
Imaging in abdominal tuberculosis, Suárez T, García V, Estrada T, Acosta F
Review Articles
b
a
Figure 13. Contrast abdominal CT of a 33 year-old male patient. (a) Axial section and (b) coronal reconstruction showing concentric and irregular thickening
of the distal ileum, the ileocecal valve and the caecum (arrows), as well as pericecal valve striation (arrow head).
bloodstream. The antrum and distal corpus of the stomach are
the sites most commonly affected. Barium studies reveal two
patterns: an ulcerative pattern mimicking peptic ulcer disease,
and a hypertophic pattern mimicking a malignancy. Additionally,
adjacent lymphadenopathies may produce extrinsic compression. Complications include outflow tube obstruction and fistula
formations. The CT scan reveals regional lymphadenopathies
and submucosal masses.
Duodenal tuberculosis
This form of tuberculosis is found in 2% of all patients
with intestinal tuberculosis. It usually involves the third and
fourth portions of the duodenum. It manifests in the form of
compression secondary to adjacent lymphadenopathies, and
may become complicated with fistulae secondary to chronic
mucosal inflammation. The CT scan reveals thickening of the
duodenal folds, regional lymphadenopathies and thickening of
the mesenteric root.
Jejunal tuberculosis
The isolated involvement of the jejunum is rare and is almost
always associated with peritonitis. Imaging characteristics are
non-specific, with the presence of ulcers, thickened folds and
stenosis.
Colonic tuberculosis
Isolated colitis with no ileocecal valve involvement is rare.
It occurs in 9% of intestinal tuberculosis cases. The clinical
manifestations are non-specific and include diarrhea and weight
loss. It usually affects one colonic segment (ascending, transverse or descending). Pancolitis is unusual and it is difficult to
differentiate from ulcerative colitis (50).
Barium studies show spike formation, spasms and stiffness in the early stages. In the late stages there is stenosis and
Rev Colomb Radiol. 2010; 21:(4):1-11
fistulae formation. Ultrasound plays a very limited role due to
gas interposition, but it may show concentric mural thickening. In contrast, CT is the most useful method, revealing mural
thickening, obstruction or subobstruction secondary to stenosis,
lymphadenopathies and ascites.
Tuberculosis of the abdominal aorta and
its branches
Tuberculosis of the aorta and its branches is extremely rare.
Although any segment of the aorta may be involved due to
bloodstream spread or direct extension from adjacent lymphadenopathies, more cases have been described in the abdominal
portion (51). Likewise, the disease may manifest in the form of
arteritis with areas of stenosis or aneurysmal dilations, mainly
of the sacular type. Aortal dissections may also occur, although
less frequently.
Vascular granulomatous infection must be suspected in
patients with a history of disseminated tuberculosis and associated abdominal aneurysm. Characteristically, these aneurysms
are not associated with calcifications, unlike those of atherosclerotic origin.
Conclusion
Although the clinical and imaging manifestations of abdominal tuberculosis may mimic other pathologies, a high
degree of suspicion is required in populations at risk. The
prevalence of the disease is still high in our setting. Abdominal
manifestations of tuberculosis depend on the patient’s immune
status and they may appear late, with the resulting sequels for
the organ involved. The most acute manifestations are usually
accompanied by pulmonary infection. Imaging recognition
helps guide the clinician in the search and demonstration of
the mycobacterium.
9
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Correspondence
Tatiana Suárez
Universidad de Antioquia
Medellín, Colombia
tatisuarez@hotmail.com
Received for evaluation: September 18, 2010
Accepted for publication: October 20, 2010
Rev Colomb Radiol. 2010; 21:(4):1-11
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